| First Author | Zhang S | Year | 2018 |
| Journal | G3 (Bethesda) | Volume | 8 |
| Issue | 10 | Pages | 3377-3382 |
| PubMed ID | 30135105 | Mgi Jnum | J:278225 |
| Mgi Id | MGI:6296338 | Doi | 10.1534/g3.118.200509 |
| Citation | Zhang S, et al. (2018) Deletion of GIT1 Impacts eNOS Activity To Aggravate sFlt-1-Induced Preeclampsia Phenotype in Mice. G3 (Bethesda) 8(10):3377-3382 |
| abstractText | Preeclampsia, a serious multisystem disorder specific to human pregnancy, remains a considerable burden of disease worldwide. Reduced nitric oxide bioavailability is proved to be crucial in the maternal and fetal pathophysiology of preeclampsia. G-protein-coupled Receptor Kinase Interactor-1 (GIT1) is a novel endothelial nitric oxide synthases (eNOS) interactor mediator. The aim of this paper is to investigate the effect of GIT1 on preeclampsia. Blood pressure (BP) was measured using a carotid catheter-calibrated eight-chamber tail-cuff system (CODA) at the same time daily. Urinary albumin excretion (UAE) was determined using Albuwell-M kits (Exocell Inc) and creatinine clearance (CCr) was determined by measuring urinary creatinine concentration with tandem liquid chromatography-mass spectrometry. The release of nitrite was analyzed to detect nitric oxide (NO) production using a Sievers Chemiluminescence NO Analyzer. NOS activity was examined by measuring the conversion of (3)H-labeled l-arginine to (3)H-labeled l-citrulline. BP was significantly increased in GIT1(-/-) mice with or without sFIT-1 treatment. In addition, GIT1-/- mice possessed higher UAE and lower CCr. Depletion of GIT1 impedes the NO production and placenta eNOS activity. Additional GIT1 attenuates sFlt-1-induced preeclampsia phenotypes. Our findings suggest that GIT1 significantly extenuates the sFlt-1-induced preeclampsia phenotypes by inhibiting eNOS activity, indicating a crucial role of GIT1 in the progression of preeclampsia. |
